A gastrointestinal hormone, cholecystokinin (CCK), has been regarded as a putative satiety hormone which is involved in the regulation of food intake. In the genetically obese mice the brain activity of this hormone is lower than normal and is hypothesized to be a cause of unrestrained appetite in this strain of mice. The first aim of this project is to investigate the effect of long-term elevation of CCK on meal intake patterns and body weight in normal rats and obese rats due to aging, diet conditions, ventromedial hypothalamic lesion, ovariectomy, and genetic factors. We will see whether CCK can be used to maintain the normal level of body weight in otherwise obese rats in the free feeding condition. We will observe all aspects of meal intake to see how the lower body weight may be maintained. The second aim is to investigate the nature of CCK satiety to see whether CCK alters the palatability of food to reduce intake. Also when palatability is altered by mixing of novocain in the food what will happen to intake and body weight. We will study whether the CCK satiety needs peripheral ingestive cues to become effective. The third aim is to study whether the CCK satiety is specific to the fat and protein containing food but with no effect on suppressing sugar intake and also the food intake elicited by 2DG injection (sugar-related hunger). The fourth aim is to study whether a food flavor can become conditioned to the CCK satiety effect to control the amount of food intake. The results will provide us with useful strategies toward the management of food intake in clinical situations.